Anesthesia and Liver Diseases
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9.1.09ANAESTHESIA AND LIVER DISEASEDr.Pratheeba Durairaj ,M.D,D.A,
Liver FunctionsThe liver conjugates bilirubin, produced from the degradation of the haemoglobin
- water-soluble form of bilirubin is then excreted into the bile ducts The bile salts produced by the liver are passed to the gut - necessary for the absorption of the fat-soluble vitamins A, D, E and K. Synthesis of proteins - most clotting factors, albumin. Lipid metabolism - cholesterol and triglycerides synthesised here. Carbohydrate metabolism - synthesis and breakdown of glycogen . It stores glycogen and releases glucose into the blood when the blood glucose falls for any reason.Biotransformation of drugs either by oxidation or conjugation - render them water-soluble - more easily excreted.
Impaired liver function Direct effectsHypoglycemia, Lactic acidosis , Hyper metabolism, Azotemia and Impaired urea synthesis. Jaundice appears when serum bilirubin exceeds 35 mol/l Defects in cholesterol metabolism together with intra-hepatic cholestasis may lead to production of poor quality bile and malabsorbtion of fat and fat-soluble vitamins. Reduced synthesis of proteins such as albumin, clotting factors, thyroid binding globulin and pseudo-cholinesterase. Impaired hormone biotransformation, reduced production of modulator proteins and reduced protein binding lead to increased circulating levels of hormones such as insulin, thyroxine, T3, aldosterone and oestrogen
Indirect effects Cardiovascular changesVasodilatation and vascular shunting are almost invariable in ESLD. Low systemic vascular resistance (SVR) results in high cardiac output and high mixed venous oxygen saturationsIntrapulmonary & arteriovenous shunting Pulmonary hypertension may developTachycardia, bounding pulse ,Ejection systolic murmur
Pulmonary problems are both vascular and mechanical. Hepato-Pulmonary syndrome triad of end stage liver disease, A-a gradient >2 kPa , intrapulmonary vascular dilationImpaired pulmonary function in absence of cardiopulmonary diseaseImpaired hypoxic vaso-constriction and ventilation perfusion mismatch lead to arterial desaturation and clubbing if chronic.Cyanosis ,dyspnoea , platypnea, orthodeoxia [desaturation pronounced in upright position relieved by recumbency ] Pleural effusions together with ascites can cause considerable mechanical embarrassment of respiration and a reduction in functional residual lung capacity.
Low GFR Low renal blood flow No other cause for renal failure Functional renal failure Symptoms water retention, Azotemia, hyponatremia, & oliguria
Hepatorenal failureCauses may be
Pre and peroperative dehydration Hypovolaemia Falls in renal blood flow during surgery, Direct effect of the excess conjugated bilirubin on the renal tubules or possibly an increased absorption of endotoxin from the gut.Not a major risk in patients with Prehepatic jaundice.
Managementof Hepato renal syndromeAvoid it developing by ensuring adequate hydration and a urine flow of at least 50mls/hr in the average adult patient. In moderately elevated bilirubin - simple fluid loading for 12 hours before surgery using 0.9% NaCl and during the operation.
If the urine output is not maintained - Mannitol 10%Bilirubin greatly elevated (>140 micromols/litre), - intravenous fluids during the 24 hours before surgery and for 36 hours postoperatively.
Mannitol 10% 0.5-1g/kg - prior to surgery without making the patient dehydrated as a result of an over-zealous diuresis.
Mechanisms leading to deepening encephalopathy -incompletely understood. Due to accumulation of neurotoxic compounds penetrating an impaired blood-brain barrier. Symptoms can occur in chronic as well as in acute disease, may be rapid in onset Precipitated by a gastrointestinal bleed, dietary protein overload or sepsis. Somnolence can be exacerbated by sedative drugs and narcotics.Rapid correction of hyponatraemia can lead to osmotic demyelination and central pontine myelinolysis and should be avoided
HAEMATOLOGICAL PROBLEMSAnaemia may be the result of nutritional deficiency, toxic bone marrow depression or gastrointestinal bleeding from varices or erosions. Coagulation defects arise from thrombocytopenia, platelet dysfunction and decreased levels of circulating clotting factors. Clotting factor levels fall because of impaired synthesis, vitamin K malabsorbtion and intravascular consumption. The short half-life of clotting factors means that INR or Prothrombin Ratio (PTR) can reliably be used to evaluate residual hepatic function.Treatment Vit K ,FFP
GASTROINTESTINAL SYSTEMRupture of oesophageal varicesVassopressin & octreotide reduce portal hypertensionSusceptibility to infection - increased
Drug dispositionCholestasis will reduce absorption of fat-soluble drugs after oral administration. Compartment changes and altered protein binding will affect volume of distribution, clearance and re-distribution. Patients with liver dysfunction may be particularly sensitive to opiates and benzodiazepines due to altered end-organ sensitivity
Effect of hepatic dysfunction on anaesthetics Albumin -increased free fraction Altered volume of distribution [Ascites & increased total body water compartment],Reduced metabolism alters drug pharmacodynamics
Opiods - Morphine ,pethidine - respiratory depression & sedation
Sedative /hypnotic drugs Benzodiazepines prolonged
NDMR Prolonged action for vecuronium and pancuronium
DMRDecreased serum cholinesterase activity
The Effect of Anaesthetics on Liver FunctionVOLATILE AGENTSHalothane - HABF/PBF, disturb HABR [hepatic arterial buffer response]Sevoflurane ,isoflurane maintain HABR SEVO > ISO > DES > HALO
IV ANAESTHETICSThiopentone /etomidate -THBFPropofol - THBF splanchnic vasodilatorKetamine no effects
REGIONAL ANAESTHESIAHigh epidural may reduce THBF
Effect of General Anaesthesia on liver functions in patients with preexisting liver diseasesIndian Journal of Anaesthesia. 1989 Apr; 37(2): 61-6 ABSTRACT: Effects of anaesthetics on liver functions were studies in 13 patients having no liver disease (group I) and 11 patients having liver disease (group II). Serum cholinesterase increased significantly in both the group. Rise in SGOT levels was significant only in group I, who had greater surgical trauma and not in the other group of patients (group II). Significant decrease in total serum proteins was seen on different postoperative days in group I but only on 5th postoperative day in group II. It was concluded that presence of liver disease does not increase the adverse effect of anaesthesia on liver function and that surgical trauma is more important than anaesthesia in producing liver dysfunction.
Signs of Liver DiseaseJaundiceHepatomegalySpider NaeviSplenomegalyScratch MarksAscitesPalmer Erythema
Dilated Abdominal VeinsPeripheral OedemaFinger ClubbingTesticular AtrophyBruisingGynaecomastiaConfusion/Coma
JaundicePrehepatic jaundice [haemolysis] Massive intravascular haemolysis - as in some forms of malaria or in sickle cell anemia Hepatocellular function is normal but overwhelmed - increased unconjugated bilirubin Intact Protein and carbohydrate metabolism No reduction in the absorption of Vitamin K or production of clotting factors.
Hepatocellular jaundice Hepatitis or Cirrhosis decreased protein synthesis, signs of delayed clotting, and even encephalopathy.
CONTDObstructive JaundiceBiliary obstruction - from a stone in the common bile duct, pancreatic tumour or ascending cholangitis Hepatocellular function is normal Excess plasma bilirubin is chiefly conjugated - excreted in the urine which becomes dark. Stools are pale as a result of poor lipid absorption. Protein synthesis is normal Vitamin K dependant clotting factors reduced
as the absorption of vitamin K is dependent on the excretion of bile salts into the small intestine clotting time prolonged parenteral vitamin K.
Renal impairment in Jaundice
Release of endotoxins into systemic circulation
following biliary obstruction renal failurePrevention
- in high sr.bilirubin levels percutaneous drainage of biliary tree under antibiotic cover - pre op oral bile salts - post op RF
Liver Function Tests
Indication of severity, help to differentiate between prehepatic, hepatocellular and obstructive jaundice.Jaundice - sign of an elevation of serum bilirubin. Protein and albumin levels are normal in prehepatic or obstructive jaundice, low values indicate hepatocellular damage.clotting - Prothrombin Time An elevated INR may indicate impaired synthesis of clotting factors due to hepatocellular damage or malabsorption of vitamin K due to biliary obstruction.
ContdProthrombin time[ half life - 6 -12 hrs ] best indicator than Albumin [ half life 24 -48 days]Alanine Transaminase (ALT) and Aspartate Transaminase (AST) are enzymes that are released into the circulation by damaged hepatocytes. Raised levels indicate hepatocellular damage. AST can also be elevated in other circumstances such as myocardial infarction Alkaline Phosphatase (ALP) is an enzyme localized near the bile cannaliculi and is elevated in biliary obstruction. Not specific to hepatobiliary disease,[ raised in malignant bone disease]. An accompanying rise in Gamma glutamyl Transferase (Gamma GT) suggests that the ALP is from the liver.
ContdGlutathione S transferase to assess